| In Vitro |
CAY10526 (5 μM; 1 h) potently inhibits NO donor-induced PGE2 production in human melanoma cell lines A375 and SB2[1].
CAY10526 (0-20 μM; 72 h) potently reduces the viability of human melanoma cell lines A375, SB2 and WM793 with high mPGES1 expression, with an IC50 < 5 μM; whereas in human melanoma cell lines SK-MEL-28, WM1361A with low mPGES1 expression and BJ fibroblasts, the activity of this compound is significantly attenuated (IC50 >10 μM)[1].
CAY10526 (5 μM; 48 h) regulates 69 proteins associated with cell death and survival, including reducing the phosphorylation level of YB-1, cyclin B1, and the anti-apoptotic proteins BCL-2/BCL-XL, while upregulating p21, the pro-apoptotic proteins BAX/BAK, and activated caspase-3 in A375 and SB2 human melanoma cells[1].
CAY10526 (1-50 μM; 12 h) inhibits the proliferation of DU-145 prostate cancer cells in a concentration-dependent manner. A significant reduction in cell viability is observed at concentrations of 10 μM and 20 μM, and the inhibitory effect reaches a plateau when the concentration exceeds 20 μM[2].
CAY10526 (10-20 μM; 12 h) downregulates mPGES-1 expression in DU-145 prostate cancer cells in a concentration-dependent manner in vitro; at a concentration of 10 μM, it maintains high expression levels of Beclin-1 compared with the complete medium control group, while at 20 μM, it significantly reduces the expression of both mPGES-1 and Beclin-1[2].
CAY10526 (1-50 μM; 18 h) potently inhibits leptin-induced PGE2 production in OE33 esophageal adenocarcinoma cells, achieving complete inhibition at concentrations of 10 μM and 50 μM[4].
CAY10526 (10 μM; 18 h) inhibits leptin-induced mPGES-1 protein expression in OE33 esophageal adenocarcinoma cells without altering COX-2 expression[4].
CAY10526 (1-50 μM; 24 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, reaching maximum inhibitory activity at 10 μM and 50 μM, which is comparable to the activity of active COX-2 inhibitors at corresponding concentrations[4].
CAY10526 (1-50 μM; 48 h) reduces the number of viable serum-cultured OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with maximal activity observed at 10 μM[4].
CAY10526 (1-50 μM; 25 h) inhibits leptin-induced increase in the number of viable OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with its maximal activity achieved at 10 μM[4].
CAY10526 (10 μM; 25 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells by targeting the upstream pathway of PGE2 production, while exogenous PGE2 restores this proliferative effect[4].
CAY10526 (10 μM; 25 h) inhibits IL-1β-induced PGE2 production and promotes PGI2 production in HUVECs, without affecting endothelial prostacyclin synthesis[4].
CAY10526 (25 h) inhibits thrombin-induced PGE2 production and promotes PGI2 production in human umbilical vein endothelial cells (HUVECs), without affecting endothelial prostacyclin synthesis[4].
CAY10526 (10-80 μM; 24-72 h) inhibits the proliferation of human T-cell lymphoma Hut78 cells, with an IC50 of 27.64 μM at 24 h, and suppresses cell viability in a dose-dependent manner after 72 h of incubation[5].
CAY10526 (10-80 μM; 24 h) reduces the expression of mPGES-1 protein in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 40 μM and 80 μM after 24 h[5].
CAY10526 (10-80 μM; 24 h) inhibits PGE2 synthesis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 10, 20, 40 and 80 μM after 24 h[5].
CAY10526 (20-40 μM; 24 h) induces apoptosis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the apoptosis rates at concentrations of 20 μM and 40 μM increase significantly after 24 h[5].
CAY10526 (20-40 μM; 24 h) upregulates the expression of activated caspase-3 in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the expression levels at 20 μM and 40 μM increase significantly after 24 h[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the JAK/STAT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of JAK1, JAK2 and p-STAT3; after 24 h, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total STAT3 level remains unchanged[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the PI3K/AKT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of PI3Kp110, PI3Kp85 and p-AKT; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total AKT level remains unchanged[5].
CAY10526 (20-40 μM; 24 h) inhibits the TGF-β/Smad3 signaling pathway in human T-cell lymphoma Hut78 cells in a dose-dependent manner by reducing the expression of TGF-β and p-Smad3; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total Smad3 level remains unchanged[5].
CAY10526 (20-40 μM; 24 h) reduces CyclinD1 expression in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 20 μM and 40 μM after 24 h[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
CAY10526 Related Antibodies
Cell Viability Assay[1]
| Cell Line: |
A375, SB2, WM793, SK-MEL-28, WM1361A human melanoma cells, BJ normal fibroblasts |
| Concentration: |
0, 1, 5, 10 and 20 μM |
| Incubation Time: |
72 h |
| Result: |
Inhibited cell viability with an IC50 < 5 μM in mPGES1-high melanoma cell lines (A375, SB2, WM793).
Showed significantly weaker activity with an IC50 >10 μM in mPGES1-low melanoma cell lines (SK-MEL-28, WM1361A) and normal BJ fibroblasts. |
Cell Proliferation Assay[2]
| Cell Line: |
DU-145 prostate cancer cells |
| Concentration: |
1, 10, 20 and 50 μM |
| Incubation Time: |
12 h |
| Result: |
Inhibited DU-145 cell proliferation in a concentration-dependent manner.
Exhibited optical density values of 0.34 at 1 μM, 0.22 at 10 μM, 0.08 at 20 μM, and 0.06 at 50 μM.
Reduced cell viability significantly at 10 μM and 20 μM compared to control.
Showed no significant difference in cell viability between 20 μM and 50 μM groups. |
Western Blot Analysis[2]
| Cell Line: |
DU-145 prostate cancer cells |
| Concentration: |
10 and 20 μM |
| Incubation Time: |
12 h (serum-free conditions) |
| Result: |
Downregulated mPGES-1 protein expression in a concentration-dependent manner.
Reduced Beclin-1 expression at 10 μM compared to serum-free group, while levels remained higher than complete medium control group.
Significantly downregulated both mPGES-1 and Beclin-1 at 20 μM. |
ELISA Assay[4]
| Cell Line: |
leptin-stimulated OE33 oesophageal adenocarcinoma cells |
| Concentration: |
1 μM, 10 μM, 50 μM |
| Incubation Time: |
60 min pretreatment, followed by 18 h leptin stimulation |
| Result: |
Caused a concentration-dependent reduction in leptin-driven, COX-2-dependent PGE2 production.
Abolished leptin-induced PGE2 production at 10 μM and 50 μM, achieving inhibition comparable to COX-2 inhibitors celecoxib and NS-398 at their active concentrations. |
Western Blot Analysis[4]
| Cell Line: |
leptin-stimulated OE33 oesophageal adenocarcinoma cells |
| Concentration: |
10 μM |
| Incubation Time: |
60 min pretreatment, followed by 18 h leptin stimulation |
| Result: |
Completely blocked leptin-induced mPGES-1 protein expression.
Left COX-2 protein expression unaffected. |
Cell Proliferation Assay[4]
| Cell Line: |
leptin-stimulated OE33 oesophageal adenocarcinoma cells |
| Concentration: |
1 μM, 10 μM, 50 μM |
| Incubation Time: |
60 min pretreatment, followed by 24 h leptin stimulation |
| Result: |
Caused a concentration-dependent decrease in leptin-stimulated OE33 cell proliferation.
Blocked leptin-induced proliferation at 10 μM and 50 μM with effectiveness matching COX-2 inhibitors celecoxib (1 μM) and NS-398 (10 μM). |
Cell Viability Assay[4]
| Cell Line: |
serum-cultured OE33 oesophageal adenocarcinoma cells |
| Concentration: |
1 μM, 10 μM, 50 μM |
| Incubation Time: |
48 h |
| Result: |
Caused a concentration-dependent reduction in viable OE33 cell numbers, with no further reduction observed at concentrations above 10 μM.
Significantly reduced viable cell numbers at all tested concentrations compared to untreated controls. |
Cell Viability Assay[4]
| Cell Line: |
leptin-stimulated OE33 oesophageal adenocarcinoma cells |
| Concentration: |
1 μM, 10 μM, 50 μM |
| Incubation Time: |
60 min pretreatment, followed by 24 h leptin stimulation |
| Result: |
Blunted the leptin-stimulated increase in viable OE33 cell numbers in a concentration-dependent manner, with no additional effect observed at concentrations above 10 μM.
Significantly reduced leptin-stimulated viable cell numbers at all tested concentrations compared to leptin-only controls. |
Cell Viability Assay[4]
| Cell Line: |
leptin-stimulated OE33 oesophageal adenocarcinoma cells (PGE2-rescue experiment) |
| Concentration: |
10 μM |
| Incubation Time: |
60 min pretreatment, followed by 24 h stimulation with leptin, PGE2, or leptin + PGE2 |
| Result: |
Allowed exogenous PGE2 to stimulate OE33 cell proliferation even in its presence.
Saw the inhibitory effect on leptin-stimulated proliferation reversed by added PGE2. |
ELISA Assay[4]
| Cell Line: |
IL-1β-stimulated human umbilical vein endothelial cells (HUVECs) |
| Concentration: |
10 μM |
| Incubation Time: |
60 min pretreatment, followed by 24 h IL-1β stimulation |
| Result: |
Effectively blocked IL-1β-driven PGE2 production in HUVECs.
Significantly enhanced IL-1β-stimulated PGI2 production, unlike COX-2 inhibitors celecoxib and NS-398 which abolished production of both PGE2 and PGI2. |
ELISA Assay[4]
| Cell Line: |
thrombin-stimulated human umbilical vein endothelial cells (HUVECs) |
| Concentration: |
10 μM |
| Incubation Time: |
60 min pretreatment, followed by 24 h thrombin stimulation |
| Result: |
Blocked thrombin-stimulated PGE2 production in HUVECs.
Significantly enhanced thrombin-stimulated PGI2 production, unlike COX-2 inhibitors celecoxib and NS-398 which abolished production of both PGE2 and PGI2. |
Western Blot Analysis[5]
| Cell Line: |
human T-cell lymphoma Hut78 cells |
| Concentration: |
10, 20, 40 and 80 μM |
| Incubation Time: |
24 h |
| Result: |
Down-regulated mPGES-1 protein expression in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 40 μM and 80 μM compared to untreated cells. |
Apoptosis Analysis[5]
| Cell Line: |
human T-cell lymphoma Hut78 cells |
| Concentration: |
20 and 40 μM |
| Incubation Time: |
24 h |
| Result: |
Significantly increased the apoptosis rate of Hut78 cells in a dose-dependent manner.
Caused statistically significant elevations at 20 μM and 40 μM compared to untreated cells. |
Western Blot Analysis[5]
| Cell Line: |
human T-cell lymphoma Hut78 cells |
| Concentration: |
20 and 40 μM
|
| Incubation Time: |
24 h |
| Result: |
Increased the expression of cleaved caspase-3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant elevations at 20 μM and 40 μM compared to untreated cells.\nDecreased the expression of JAK1, JAK2, and p-STAT3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total STAT3 expression unchanged.\nDecreased the expression of PI3Kp110, PI3Kp85, and p-AKT in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total AKT expression unchanged.\nDecreased the expression of TGF-β and p-Smad3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total Smad3 expression unchanged.\nDecreased CyclinD1 expression in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells. |
|
| Solvent & Solubility |
In Vitro:
DMSO : 66.67 mg/mL (214.26 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing
Stock Solutions
|
Concentration
Solvent
Mass
|
1 mg |
5 mg |
10 mg |
|
1 mM
|
3.2138 mL
|
16.0689 mL
|
32.1378 mL
|
|
5 mM
|
0.6428 mL
|
3.2138 mL
|
6.4276 mL
|
|
10 mM
|
0.3214 mL
|
1.6069 mL
|
3.2138 mL
|
View the Complete Stock Solution Preparation Table
*
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Molarity CalculatorDilution Calculator
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
-
Protocol 1
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline) Solubility: 2.5 mg/mL (8.03 mM); Clear solution; Need ultrasonic
This protocol yields a clear solution of 2.5 mg/mL. Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Please enter your animal formula composition:
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
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